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TGFβ

The Megakaryocytic Transcription Factor ARID3A Suppresses Leukemia Pathogenesis

[Blood] The authors reported that post-transcriptional repression of the transcription factor ARID3A by miR-125b was a key event in megakaryoblastic leukemia pathogenesis, and showed that chromosome 21-encoded miR-125b synergized with Gata1s to drive leukemogenesis in this context.

Chronic Ethanol Exposure Induces Deleterious Changes in Cardiomyocytes Derived from Human Induced Pluripotent Stem Cells

[Stem Cell Reviews and Reports] Understanding biological mechanisms involved in the long-term alcohol exposure-induced cardiotoxicity is pivotal to the discovery of therapeutic strategies. Cardiomyocytes derived from human pluripotent stem cells were treated with clinically relevant doses of ethanol for various durations up to five weeks.

Negative Regulation of TGFβ-Induced Apoptosis by RAC1B Enhances Intestinal Tumorigenesis

[Cell Death & Disease] By modeling early stages of adenoma initiation researchers observed a reduced apoptotic rate in RAC1B overexpressing tumors, suggesting protection from apoptosis as a mediator of this phenotype.

Modelling Human Liver Fibrosis in the Context of Non-Alcoholic Steatohepatitis Using a Microphysiological System

[Communications Biology] Researchers investigated how liver fibrosis and features of non-alcoholic steatohepatitis (NASH) could be modelled using an in vitro microphysiological system (MPS). The NASH MPS model comprised a co-culture of primary human liver cells, which were cultured in a variety of conditions including +/− excess sugar, fat, exogenous TGFβ or LPS.

Optogenetic Modeling of Human Neuromuscular Circuits in Duchenne Muscular Dystrophy with CRISPR and Pharmacological Corrections

[Science Advances] Investigators combined transcriptome analysis and modeling of Duchenne muscular dystrophy (DMD) patient-derived neuromuscular circuits with CRISPR-corrected isogenic controls in compartmentalized microdevices and showed that neuromuscular junction volumes and optogenetic motor neuron–stimulated myofiber contraction were compromised in DMD neuromuscular circuits.

Anti-Latent TGFβ Binding Protein 4 Antibody Improves Muscle Function and Reduces Muscle Fibrosis in Muscular Dystrophy

[Science Translational Medicine] Scientists generated a monoclonal human anti-latent transforming growth factor β binding protein 4 (LTBP4) antibody directed toward LTBP4’s hinge region. In vitro, anti-LTBP4 bound LTBP4 protein and reduced LTBP4 proteolytic cleavage. In isolated myofibers, the LTBP4 antibody stabilized the sarcolemma from injury.

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